Back to Search Start Over

Mouse Slfn8 and Slfn9 genes complement human cells lacking SLFN11 during the replication stress response

Mouse Slfn8 and Slfn9 genes complement human cells lacking SLFN11 during the replication stress response

Authors :
30281728
20894455
Alvi, Erin
Mochizuki, Ayako L.
Katsuki, Yoko
Ogawa, Minori
Qi, Fei
Okamoto, Yusuke
Takata, Minoru
Mu, Anfeng
30281728
20894455
Alvi, Erin
Mochizuki, Ayako L.
Katsuki, Yoko
Ogawa, Minori
Qi, Fei
Okamoto, Yusuke
Takata, Minoru
Mu, Anfeng
Publication Year :
2023

Abstract

The Schlafen (SLFN)11 gene has been implicated in various biological processes such as suppression of HIV replication, replication stress response, and sensitization of cancer cells to chemotherapy. Due to the rapid diversification of the SLFN family members, it remains uncertain whether a direct ortholog of human SLFN11 exists in mice. Here we show that mSLFN8/9 and hSLFN11 were rapidly recruited to microlaser-irradiated DNA damage tracks. Furthermore, Slfn8/9 expression could complement SLFN11 loss in human SLFN11⁻⁄⁻ cells, and as a result, reduced the growth rate to wild-type levels and partially restored sensitivity to DNA-damaging agents. In addition, both Slfn8/9 and SLFN11 expression accelerated stalled fork degradation and decreased RPA and RAD51 foci numbers after DNA damage. Based on these results, we propose that mouse Slfn8 and Slfn9 genes may share an orthologous function with human SLFN11. This notion may facilitate understanding of SLFN11’s biological role through in vivo studies via mouse modeling.

Details

Database :
OAIster
Notes :
English
Publication Type :
Electronic Resource
Accession number :
edsoai.on1458650436
Document Type :
Electronic Resource